Hepcidin is low in children with moderate acute malnutrition and asymptomatic malaria: Secondary analysis of a 2x2x3 factorial randomized trial in Burkina Faso

Abstract

Children with moderate acute malnutrition (MAM) have an increased risk of iron deficiency, anemia, and death from infectious diseases. The iron-regulating hormone hepcidin is increased in inflammation and may be important in regulating iron metabolism in children with MAM. Asymptomatic malaria has previously been associated with elevated s-hepcidin. We assessed the association between inflammation, iron status, anthropometry, and malaria and serum hepcidin (s-hepcidin) and evaluated the effect of food supplementation on s-hepcidin in a secondary analysis in 1019 children with MAM from a randomized intervention trial in Burkina Faso. Children received 12 weeks supplementation of 500 kcal/day as either corn-soy blend (CSB) or lipid-based nutritional supplements (LNS). S-hepcidin was measured at baseline and after 12 weeks. At baseline, correlates of s-hepcidin were determined using tobit regression. The effect of supplementation was determined using mixed effects tobit regression. Children with iron deficiency had 82% (95%CI 76; 87) lower s-hepcidin than those without, whereas children with acute infection and inflammation had elevated s-hepcidin. Children with symptomatic malaria had 103% (95%CI 32; 210) higher s-hepcidin than afebrile children without detectable malaria while children with recent or asymptomatic malaria had 51% (95%CI 35; 63) lower s-hepcidin. S-hepcidin increased 61% (95%CI 38; 87) after 12 weeks food supplementation with 22% higher (95% CI 2; 45) concentration in those who received LNS compared with CSB. Expectedly, morbidity and inflammation were associated with higher, and iron deficiency with lower, s-hepcidin. Further studies are needed to corroborate the finding of decreased s-hepcidin in malnourished children with asymptomatic malaria.